Premium
Moderate exercise improves the metabolic response to a fat/sugar overload but exacerbates cardiac damage
Author(s) -
Pohlman Roberta L,
Alghamri Mahmoud S,
Bechara Ana Carolina C,
Hartzler Lynn,
Mirkin L David,
Farah Vera,
Morris Mariana
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1057.15
Subject(s) - sed , medicine , endocrinology , glycogen , fructose , ex vivo , cardiac function curve , insulin , chemistry , biochemistry , heart failure , in vitro
A western diet, high in fat and sugar, causes metabolic and cardiovascular dysfunction. The objective was to determine the effect of moderate swimming exercise (1 hr/d, 3 d/wk, n = 9–10/group) on the metabolic and cardiac responses to a high fat/sugar diet in mice. Groups are: Control (CON); Sedentary (SED, fat/fructose) and Exercise (EX, fat/fructose). Chow (60% fat) and fructose water (10%) were given ad libitum for 8 wk. Parameters measured were body fat, heart function (echocardiography, Echo), glucose, glucose tolerance (GTT) and liver glycogen. Mice gained body fat (up to 45%) on the fat/fructose diet with no difference between groups. Metabolic function was improved in the EX group as determined by glucose (SED>EX p <0.01) and GTT (SED>EX, p< 0.05). Insulin was lower in EX than SED, suggesting improvement in function. The diet increased liver glycogen, an effect which was improved in the EX group. Echo measurements showed impairment in cardiac function in the EX group. Relative wall thickness was higher in EX vs SED (0.35±0.01 vs 0.29 ±0.01, p <0.01). Fractional shortening was reduced in EX group (EX 0.31±0.01 vs SED 0.36±0.01, p < 0.01). This resulted in a reduced ejection fraction of ~37% vs 49% (EX vs SED). Data demonstrate that a moderate exercise paradigm combined with a high fat/sugar diet improves metabolic function but is detrimental to heart function in morbidly obese mice. Supported by NIH R01 HL093567